Key result
Decreased dopamine receptor function and increased reactive oxygen species production, working in concert or independently, contribute to the pathogenesis of essential hypertension.
This review highlights the interplay between decreased dopamine receptor function and increased reactive oxygen species in the pathogenesis of essential hypertension.
Supports dopamine-ROS interplay in essential hypertension pathogenesis; leaves open whether targeting these pathways improves outcomes.
Essential hypertension is a major risk factor for stroke, myocardial infarction, and heart and kidney failure. Dopamine plays an important role in the pathogenesis of hypertension by regulating epithelial sodium transport and by interacting with vasoactive hormones and humoral factors. However, the mechanisms leading to impaired dopamine receptor function in hypertension states are not clear. Compelling experimental evidence indicates a role of reactive oxygen species (ROS) in hypertension, and there are increasing pieces of evidence showing that in conditions associated with oxidative stress, which is present in hypertensive states, dopamine receptor effects, such as natriuresis, diuresis, and vasodilation, are impaired. The goal of this review is to present experimental evidence that has led to the conclusion that decreased dopamine receptor function increases ROS activity and vice versa. Decreased dopamine receptor function and increased ROS production, working in concert or independent of each other, contribute to the pathogenesis of essential hypertension.
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Zeng et al. (2009) conducted a review in Essential hypertension. Reactive oxygen species (ROS) and dopamine receptor function was evaluated. Decreased dopamine receptor function and increased reactive oxygen species production, working in concert or independently, contribute to the pathogenesis of essential hypertension.
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